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Chronic diabetes mellitus induced in rats by streptozotocin or of genetic origin in Db/Db mice is associated with a loss of capillaries, arteriolar constriction, and a decrease in resting and maximum blood flow. As a result of these vascular changes, as well as glycolysation of hemoglobin, it is possible that tissue Po2 is reduced at rest and cannot be substantially increased during dilatation. Tissue Po2 in the intestinal muscle layer was measured at rest and during maximal dilation. In addition, the spacing between capillaries with active flow and the velocity of red blood cell flow in capillaries were measured at rest and at maximum dilation. These measurements were made in normal and diabetic rats (streptozotocin) at age 26-30 weeks; the diabetic animals had been hyperglycemic (greater than 350 mg/100 ml) for 12-15 weeks. Tissue Po2 at a distance of about 15 microns from the arterial, mid-point, and venous end of capillaries in normal rats was 24.8 +/- 1.1 (SE), 23.1 +/- 1.2, and 22.4 +/- 0.9 mm Hg, respectively, compared with 25.8 +/- 0.9, 24.1 +/- 1.2, and 22.4 +/- 1.1 mm Hg, respectively, in diabetic rats. The maximum mid-capillary tissue Po2 during dilation was 27.7 +/- 1.3 mm Hg in normal rats and 29.7 +/- 1.5 mm Hg in diabetic rats. The average distance between capillaries was 37.6 +/- 2.0 microns in normal rats and 46.8 +/- 2.9 microns in diabetic animals; vasodilation did not change the capillary spacing in either group of animals. Capillary red cell velocity in normal rats increased from 0.98 +/- 0.11 mm/sec at rest to 2.1 +/- 0.4 mm/sec during dilatation. For comparable conditions in diabetic rats, the velocities were 0.41 +/- 0.07 and 1.06 +/- 0.19 mm/sec. The data presented indicate that the diabetic animals have tissue Po2 equivalent to those in normal rats, both at rest and during maximum vasodilation. The loss of capillaries and decreased resting and maximum capillary red cell velocity in diabetic rats would decrease the delivery of oxygen, but, apparently, a decrease in oxygen consumption occurred that allowed the intestinal tissue to have a normal Po2.

Tissue PO2 in the intestinal muscle layer of rats during chronic diabetes.